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ENDO 2 Exam II (2017) > Pales diabetes intro > Flashcards

Pales diabetes intro Flashcards

1
Q

Diabetes Mellitus

A

Cluster of heterogeneous disorders with elevated blood glucose levels as a common diagnostic feature
Type 1
Type 2
Other

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2
Q

Insulin effect – anabolic effect

A

Stimulates: glucose transport, glycolysis, glycogen synthesis, amino acid transport, protein synthesis, triglyceride uptake, lipogenesis

inhibits:
glycogen breakdown, gluconeogenesis, protein breakdown, lipolysis, fatty acid oxidation

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3
Q

Type 1 DM

A

Associated with autoimmune antibodies
Likely T-Cell mediated
Requires environmental trigger
Mechanism is still not clearly understood

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4
Q

Antibodies in type 1 diabetes

A 
Glutamic acid decarboxylase 65 (GAD 65) 
Insulin antibodies (IAA)
Islet cell (ICA)
Zinc transporter 8 (ZnT8)
Tyrosine phosphatase (IA-2)

HLA-DR3, DR4

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5
Q

Type 1 DM. Prognosis

A

In the absence of renal disease, life expectancy in the United States is comparable to that of the general population.
Mortality rate of all type 1 diabetic patients from age 35 onward is about twice as high as in non-diabetics
Large reductions in the incidence of diabetes-related complications between 1990 and 2010 in the U.S due to change in management

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6
Q

Type 2 DM. Epidemiology

A

One of the most common chronic diseases,
25 million people in the US.
Prevalence increasing

Higher among Adults 65 years and older
Non-Hispanic blacks
Hispanics
American Indians

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7
Q

Type 2 DM. Mechanisms

A

Impaired Insulin Secretion

  • Decreased b-Cells Mass
  • Decreased glucose sensing by b-Cells

Impaired Insulin Action (Insulin resistance)

  • In peripheral tissues- reduced glucose uptake in muscle and fat
  • In the liver- Reduced suppression of hepatic glucose production.

Associated with:
Obesity
Metabolic syndrome
Polycystic ovary syndrome.

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8
Q

Type 2 DM. Genetics

A

Polygenic and multifactorial

More than 50 genetic risk loci identified which explain only 15% of the heritability

Emerging evidence of epigenetic changes playing a role (modification of gene expression)

“Metabolic programming” may occur in utero, with both fetal starvation and fetal overnutrition predisposing to diabetes in adult life.

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9
Q

DM Type 2 and Obesity

A

Obesity is the single most important clinical predictor of type 2 diabetes

There is a linear relationship between BMI and type 2

Related factors increasing risk

  • Sedentary lifestyle
  • Diet high in high-glycemic index food, transand saturated fats
  • Visceral adiposity (including NASH)
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10
Q

DM Type 2 and Obesity. Suggested mechanisms

A

Increase in circulating FFA interferes with Insulin action in muscles and liver
Adipose tissue macrophages produce pro-inflammatory cytokines, which can interfere with insulin signaling.
Reduced levels of the fat-derived peptide diponectin, (has both anti-inflammatory and insulin-sensitizing properties).
Lipid accumulation in pancreatic islets may lead to impaired insulin secretion.

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11
Q

Metabolic Syndrome

A

2 physical findings and 3 labs
Waist circumference > 40 inches in men
> 35 inches in women

Hypertension > 130/85 mmHg

Triglycerides > 150 mg/dL
HDL-C under 40 mg/dL in men
under 50 mg/dL in women
Glucose > 100 mg/dL

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12
Q

differences betw Type I and Type II

A

Type I: onset in childhood, relatively rare, onset acute and severe, very low insulin secretion and normal insulin sensitivity, permanent insulin dependence, all racial groups, mostly sporadic cases, no acanthosis nigricans, autoimmune etiology, goes with other autoimmune and endocrine conditions

Type II: pubertal onset, most diabetes, often insidious onset, variable insulin secretion, decreased sensitivity, temporary insulin dependence, groups of color at more risk, strong genetic component (polygenic), ACANTHOSIS NIGRICANS, not autoimmune, goes with hypertension, dyslipidemia, metabolic syndrome, polycystic ovary syndrome

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13
Q

MODY

A

mature onset diabetes of hte young

MODY 3 is most common

usually good control with sulfonylurea

usually monogenetic

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14
Q

differences between one patient’s example of MODY and type 1

A

strong family history (2 or 3 generations)
no ketoacidosis when off insulin for 3 weeks
negative pancreatic autoantibodies
detectable C-peptide levels

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15
Q

comparison between type 2 and MODY

A

type 2: polygenic, usually over 40 years, rarely seen across generations, variable penetrance, usually obese, usually have metabolic syndrome

MODY- monogenic, autosomal dominant. Usually under 25 years old, seen across generations, 80-90% penetrance, non-obese, no metabolic syndrome

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16
Q

what is the main factor in MODY?

A

The MODY syndromes involve impaired glucose induced secretion of insulin
and most work by abnormal nuclear transcription factors .

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17
Q

MODY 5 is associated with

A

renal cysts, genital tract malformations and hyperuruicemia

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18
Q

Other Types of Diabetes rather than Type 1, Type 2, MODY

A
  1. Mutant insulins (rare), and mutant Insulin receptors (Acanthosis Nigricans and extreme insulin resistance).
  2. Mutation of Mitochondrial DNA – abnormal tRNA gene with beta-cell failure– hearing loss – resembles type 1 – no autoimmunity.
  3. Wolfram syndrome – DIDMOAD – altered endoplasmic reticulum of beta-cell protein leading to apoptosis.
  4. Autosomal Recessive syndromes – Pancreatic transcription factors - neonatal or childhood - Mitchell-Riley syndrome
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19
Q

DM secondary to other causes

A
  1. Endocrinopathies (the Omas, eg. glucagonoma)- tumors secreting GH, catecholamines, glucagon, glucocorticoids, and somatostatin.
  2. Immune mediated – receptor antibodies, “Stiffman syndrome”
  3. Medications – cyclosporine, tacrolimus, steroids, thiazides, beta-blockers, olanzopine
  4. Diseases of the exocrine pancreas – pancreatitis, cystic fibrosis, etc
  5. Infections – CMV, congenital Rubella
  6. Other genetic syndromes – Downs, Turners, Klinefelters, Friedreich’s ataxia
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20
Q

Drugs producing Hyperglycemia

A

Banting HAS TO PIN

Beta blockers
Hormones (glucocortoids, glucagon, GH), HAART (PIs, NRTI)
Hyperstat (diazoxide)
Alcohol, Antipsychotics (resperidone, quetipine, olanzapine)
Sympathomimetics (norepinephrine or epinephrine), Statins
Thiazides, Tricyclics
Oral contraceptives, Opiates,
Phenytoin, Pentamidine
Indocin, Isoniazid, and Immunosuppressants (cyclosporine,
tacrolimus, sirolimus, calcineuron inhibitors)
Niacin

21
Q

Diagnosis of DM

A

Normal:
Fasting plasma glucose (FPG) under 100 mg/dL
Two-hour glucose during OGTT under 140 mg/dL (7.8 mmol/L).
HbA1c under 5.7

Pre-diabetes:
Impaired fasting glucose (IFG)
Fasting plasma glucose between 100 and 125 mg/dL.
Impaired glucose tolerance (IGT)
Two-hour plasma glucose value during a 75 g oral glucose tolerance test between 140 and 199 mg/dL.
HbA1C— persons with 5.7 to 6.4 percent are at highest risk

Diabetes mellitus :
On two different occasions FPG at or above 126 mg/dL
Two-hour value in an OGTT (2-h PG) at or above 200 mg/dL
On two different occasions random plasma glucose concentration ≥200 mg/dL in the presence of symptoms
If 2 of the above present, no need for two separate occasions
HbA1c – >6.4

22
Q

Clinical Manigestation of DM

A 
Could be asymptomatic
Polydipsia
Polyuria
Weight Loss
Acute complications of Diabetes
Chronic Complications of Diabetes
23
Q

Diabetic Ketoacidosis (DKA)

A

Hyperglycemia > 250 mg/dL
Acidosis with blood pH under 7.3
Serum bicarbonate under 15 mEq/L
* Serum positive for ketones (not just urine ketones)

24
Q

DKA develops when?

A

Only develops in the insulin deficient states

Type I DM:
Usually initial presentation
Insulin non-compliance
Increase in anti-insulin hormones (cortisol etc) during stress (infection, surgery etc.)

Type II DM:
Late stages of Beta-Cells failure
During stress

(super high glucose can also shut down pancreatic insulin producing cells)

25
Q

DKA. Clinical Presentation.

A 
Mortality rate is 5-20%
Onset over 1-2 days
Polyuria-polydipsia
Weakness
Decreased appetite/nausea/vague abdominal pain
Mental status changes
- Confusion
- Lethargy
- Coma/convulsions
26
Q

DKA. Physical Exam

A

Depending on severity

Signs of acidosis

  • Confusion
  • Lethargy
  • Kussmal Respiration
  • Fruity breath odor (acetone)

Signs of dehydration

  • Oral membranes
  • Turgor of skin
  • Hypotension/tachycardia
27
Q

DKA. Labs

A 
High Blood Glucose (350-900)
Low CO2/Bicarb/pH
High Ketones/Acetone/Ketoacids
High BUN and Creatinine
High Serum K with decrease total body K
Low Na (remember to correct it for high glucose (1 for each 100 over 100)
High phosphorus
In severe cases, signs of end organ damage maybe present.
28
Q

DKA. Treatment.

A

I.V. Insulin*****
I.V. Fluids (typically 100 ml/kg water deficit)
Electrolytes replacements
Ventilatory support in severe cases
Switch iv insulin to subq injections upon resolution of DKA
Normalization of anion gap is the most important indicator of resolution of DKA (as bicarb may remain low due to non-gap anion gap acidosis)
Look for underlying reason to prevent it in the future

29
Q

Hyperosmolar Hyperglycemic Non-ketotic state

A 
Hyperglycemia > 600 mg/dL. 
Serum osmolality > 310 mosm/kg. 
No acidosis; blood pH above 7.3. (because normal insulin)
Serum bicarbonate > 15 mEq/L. 
Normal anion gap (under 14 mEq/L).
30
Q

Hyperosmolar Hyperglycemic Non-ketotic state : progression

A 
Hyperglycemia--> osmotic diuresis --> dehydration --> increased osmolality, decrease in free fluid --> hyperglycemia (solute concentration)
Hypovolemic shock
End organ damage
- Coma
- Renal Failure
31
Q

who ends up in Hyperosmolar Hyperglycemic Non-ketotic state

A

Only type II diabetes (type I would be in DKA before they get to this state)

Older patients with poor care, dementia, etc.
Due to
- non-compliance with medications
- Acute infection/stress
- Inability to increase oral intake in response to increase urinary output

32
Q

Hyperosmolar Hyperglycemic Non-ketotic state onset

A

Insidious onset
Lethargy
On exam severe state of dehydration (around 15% of ECF loss)
Labs: very high glucose, no acidosis (unless lactic acidosis develops), K low, Na can be low, but more often high (corrected for glucose), elevated BUN/CR

33
Q

Hyperosmolar Hyperglycemic Non-ketotic state- treatment

A 
I.V. fluids*****
Some iv insulin
Electrolyte replacement
Ventilatory support needed at times
Look for underlying reason to prevent it in the future
34
Q

Hypoglycemic coma

A

Initial symptoms can start with blood glucose less than 80
If patients have had high blood glucose for a long time, even normal glucose may cause some of the hypoglycemic symptoms
Coma/passing out only if blood glucose is less than 50.
Long term diabetics or patients on beta blockers may not have any initial symptoms until they pass out (hypoglycemia unawareness)

35
Q

hypoglycemic coma- symptoms

A 
hungry
headachy
sweaty
shaky
confused
dizzy
grumpy
anxious
fast heartbeat

(remember: beta blockers can mask many of these symptoms)

36
Q

hypoglycemic signs

A

Sympathoadrenal signs(glucose under 60 mg/dL) = sweating, tachycardia, tachypnea, anxiety, tremulousness, and nausea. More common in post prandial (PP) hypoglycemia.

Neuroglycopenic signs(glucose under 50 mg/dL) = blurred vision, fatigue, dizziness, headache, confusion, seizures, coma, death. More common in fasting hypoglycemia.

37
Q

Hypoglycemic Coma treatment

A 
Sugar orally if able or iv D50
Glucagon SQ injection
Review the causes
- Too much medication
- Skipped meal
- Exercises
38
Q

Insulinoma

A

Usually age 50-70
Insulin-secreting tumors of pancreatic origin
Incidence of 1 to 4 per million.
90% are benign, solitary, intrapancreatic and less than 2 cm in diameter.
Classically, symptoms are during fasting state or following exercise.
Solitary tumor or associated with MEN 1
5 to 10% are malignant.

39
Q

Post-prandial Hyperinsulinemic Hypoglycemia (PPHH)

A

Dumping Syndrome.

PPHH After Gastric Bypass Surgery.
Insulin Autoimmune Syndrome (Hirata’s disease)
PPHH from insulin-receptor gene mutation.

40
Q

Dumping Syndrome.

A

Precipitous emptying of hyperosmolar carbohydrate-containing solutions into the small bowel –> rapid glucose absorption –> hyperglycemia –> and reactive hypoglycemia.

41
Q

PPHH After Gastric Bypass Surgery.

A

Enhanced postprandial insulin secretion from increased secretion of incretins

42
Q

Insulin Autoimmune Syndrome (Hirata’s disease)

A

antibodies to endogenous insulin.
Meal load –> hyperglycemia (antibodies bind insulin decreasing its bioavailabilty) –> high insulin level –> hypoglycemia (when insulin is released from antibodies binding)

43
Q

PPHH from insulin-receptor gene mutation.

A

Decreased degradation of insulin

44
Q

Noninsulinoma Pancreatogenous Hypoglycemia Syndrome (NIPHS)

A

Postprandial hypoglycemia
No fasting hypoglycemia
Island cell hyperplasia without a tumor
Cause and mechanism is unknown

45
Q

Non–Islet Cell Tumor Hypoglycemia(IGF-2-oma)

A

Syndrome of hypoglycemia associated with non- insulinoma neoplasm.
Hepatomas, fibromas, fibrosarcomas, others
Overproduction of IGF-2 by the tumor
Mimics the fasting hypoglycemia characteristic of insulinoma
Insulin level is low

46
Q

Hypoglycemia work up

A

72 hour fast (less if symptomatic hypoglycemia)

  • Q6h tests for glucose, insulin, C-peptide, and β-hydroxybutyrate
  • At the end of the 72 hr, inject glucagon and measure plasma glucose every 10 minutes three times

Mixed Meal Diagnostic test
After overnight fast and morning meal, check glucose, insulin, C-peptide, and proinsulin every 30 minutes for 5 hours after meal.

47
Q

Whipple’s Triad

A

Symptoms and signs of hypoglycemia

Low glucose at the time of the event (< 50 mg/dL)

Reversal with correction of the hypoglycemia

48
Q

Hypoglycemia work up

A 
Insulin antibodies.
Imaging for suspected insulinoma
 CT 
- MRI 
- Endoscopic ultrasonography (EUS)
- Arterial stimulation venous sampling
- Intraoperative ultrasonography

ENDO 2 Exam II (2017) (19 decks)

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